Cerebral evoked potentials after rectal stimulation

We obtained reproducible cortical evoked potentials (EPs) in response to electrical stimulation of the rectum with 1 Hz frequency. We found 2 distinctly different EPs in response to rectal stimulation. In 5 females, the EP had an early onset latency (mean 26 msec) with multiple positive and negative peaks. In 10 females, the EP had a later onset latency (mean 52 msec) and a trifid configuration, having a very prominent negative peak. The early onset EPs after rectal stimulation appeared very similar to the wave form of the cortical EPs recorded after pudendal nerve stimulation. Finding similar interpeak latencies in the early onset EP after rectal stimulation and the EP after pudendal nerve stimulation suggests that either the same pathway was used or that rectal stimulation also stimulated the pudendal nerve. It appears that we stimulated visceral afferents when we recorded late onset EPs, because the large EP amplitude declined rapidly with faster stimulation rates and also with greater number of averaging, and the sensation threshold was very unstable, all different to somatosensory EPs.     

Growth and differentiation of PC6 cells: the effects of pulsed electromagnetic fields (PEMF)

Previous studies in our laboratory showed that neurite outgrowth in vitro and nerve regeneration in vivo were stimulated by 2 Hz, 0.3 mT (3 G) pulsed electromagnetic fields (PEMF). To learn more about the effects of PEMF on nerve cells, we exposed PC6 cells, a standard neuronal-like cell model, to the same pulsed electromagnetic fields for 2 h/day for 2 days and asked whether two different cell processes, proliferation and differentiation, were affected. The cells were also treated with a differentiating agent, nerve growth factor (NGF), to further define any interactive effects. We found that proliferation was unaffected by either PEMF or NGF alone or in combination. Differentiation, expressed as neurite outgrowth, was strongly upregulated with NGF, but this NGF response was significantly depressed in cells treated with PEMF.     

In vivo conditions induce faithful encoding of stimuli by reducing nonlinear synchronization in vestibular sensory neurons

Previous studies have shown that neurons within the vestibular nuclei (VN) can faithfully encode the time course of sensory input through changes in firing rate in vivo. However, studies performed in vitro have shown that these same VN neurons often display nonlinear synchronization (i.e. phase locking) in their spiking activity to the local maxima of sensory input, thereby severely limiting their capacity for faithful encoding of said input through changes in firing rate. We investigated this apparent discrepancy by studying the effects of in vivo conditions on VN neuron activity in vitro using a simple, physiologically based, model of cellular dynamics. We found that membrane potential oscillations were evoked both in response to step and zap current injection for a wide range of channel conductance values. These oscillations gave rise to a resonance in the spiking activity that causes synchronization to sinusoidal current injection at frequencies below 25 Hz. We hypothesized that the apparent discrepancy between VN response dynamics measured in in vitro conditions (i.e., consistent with our modeling results) and the dynamics measured in vivo conditions could be explained by an increase in trial-to-trial variability under in vivo vs. in vitro conditions. Accordingly, we mimicked more physiologically realistic conditions in our model by introducing a noise current to match the levels of resting discharge variability seen in vivo as quantified by the coefficient of variation (CV). While low noise intensities corresponding to CV values in the range 0.04-0.24 only eliminated synchronization for low (<8 Hz) frequency stimulation but not high (>12 Hz) frequency stimulation, higher noise intensities corresponding to CV values in the range 0.5-0.7 almost completely eliminated synchronization for all frequencies. Our results thus predict that, under natural (i.e. in vivo) conditions, the vestibular system uses increased variability to promote fidelity of encoding by single neurons. This prediction can be tested experimentally in vitro.     

Simultaneous monitoring of acetylcholine and catecholamine release in the in vivo rat adrenal medulla

To simultaneously monitor acetylcholine release from pre-ganglionic adrenal sympathetic nerve endings and catecholamine release from post-ganglionic adrenal chromaffin cells in the in vivo state, we applied microdialysis technique to anesthetized rats. Dialysis probe was implanted in the left adrenal medulla and perfused with Ringer's solution containing neostigmine (a cholinesterase inhibitor). After transection of splanchnic nerves, we electrically stimulated splanchnic nerves or locally administered acetylcholine through dialysis probes for 2 min and investigated dialysate acetylcholine, choline, norepinephrine and epinephrine responses. Acetylcholine was not detected in dialysate before nerve stimulation, but substantial acetylcholine was detected by nerve stimulation. In contrast, choline was detected in dialysate before stimulation, and dialysate choline concentration did not change with repetitive nerve stimulation. The estimated interstitial acetylcholine levels and dialysate catecholamine responses were almost identical between exogenous acetylcholine (10 microM) and nerve stimulation (2 Hz). Dialysate acetylcholine, norepinephrine and epinephrine responses were correlated with the frequencies of electrical nerve stimulation, and dialysate norepinephrine and epinephrine responses were quantitatively correlated with dialysate acetylcholine responses. Neither hexamethonium (a nicotinic receptor antagonist) nor atropine (a muscarinic receptor antagonist) affected the dialysate acetylcholine response to nerve stimulation. Microdialysis technique made it possible to simultaneously assess activities of pre-ganglionic adrenal sympathetic nerves and post-ganglionic adrenal chromaffin cells in the in vivo state and provided quantitative information about input-output relationship in the adrenal medulla.     

Modulatory Inputs on Sympathetic Neurons in the Rostral Ventrolateral Medulla in the Rat

1. The first part of this study looks at spontaneously active neurons located in the rostral ventrolateral medulla (RVLM) with projections to the thoracic spinal cord. Sixteen neurons were intracellularly recorded in vivo. Four out of 16 neurons were antidromically activated from the thoracic spinal cord (axonal conduction velocities varied from 1.8 m/s to 9.5 m/s).2. The simultaneous averages of the neuronal membrane potential and arterial blood pressure triggered by the pulsatile arterial wave or the EKG-R wave demonstrated changes in membrane potential (hyperpolarization or depolarization) locked to the cardiac cycle in four neurons in this group. These neurons (three of them bulbospinal) were further tested for barosensitivity by characterizing the responses to electrical stimulation of the aortic depressor nerve. Four neurons responded with inhibitory hyperpolarizing responses characterized as inhibitory postsynaptic potentials (IPSP) to aortic nerve stimulation (onset latency: 32.3 ± 5.0 ms; mean ± SEM).3. In two neurons in the RVLM, one of them characterized as barosensitive, electrical stimulation of the opposite RVLM (0.5 Hz, 1.0 ms pulse duration, 25–100 A) elicited excitatory postsynaptic potentials (EPSPs) with latencies of 9.07 and 10.5 ms. At resting membrane potential, the onset latency of the evoked EPSPs did not change with increasing stimulus intensities. Some of the recorded neurons were intracellularly labelled with biocytin for visualization. They were found in the RVLM.4. These experiments in vivo would support the idea of a functional commissural pathway between the RVLM of both sides.5. Anatomical data have shown that some of those commissural bundle fibers originate in the C1 adrenergic neuronal group in the RVLM. In the second part of this study, we used an intracellular recording technique in vitro to investigate the effects of the indirect adrenergic agonist tyramine on neurons in the RVLM with electrophysiological properties similar to premotor sympathetic neurons in vivo.6. Tyramine (0.5–1 mM) produced a pronounced inhibitory effect with hyperpolarization and increase in membrane input resistance on two neurons characterized as regularly firing (R), and on one neuron characterized as irregularly firing (I). This effect was preceded by a transient depolarization with increases in firing rate.7. These results would indicate that neurons in the RVLM recorded in vitro and with properties similar to premotor sympathetic neurons can be modulated by catecholamines released from terminals probably making synaptic contacts.     

Brain stem mechanisms underlying acupuncture modality-related modulation of cardiovascular responses in rats.

The present study was designed to investigate brain stem responses to manual acupuncture (MA) and electroacupuncture (EA) at different frequencies at pericardial P (5-6) acupoints located over the median nerve. Activity of premotor sympathetic cardiovascular neurons in the rostral ventral lateral medulla (rVLM) was recorded during stimulation of visceral and somatic afferents in ventilated anesthetized rats. We stimulated either the splanchnic nerve at 2 Hz (0.1-0.4 mA, 0.5 ms) or the median nerve for 30 s at 2, 10, 20, 40, or 100 Hz using EA (0.3-0.5 mA, 0.5 ms) or at approximately 2 Hz with MA. Twelve of 18 cells responsive to splanchnic and median nerve stimulation could be antidromically driven from the intermediolateral columns of the thoracic spinal cord, T2-T4, indicating that they were premotor sympathetic neurons. All 18 neurons received baroreceptor input, providing evidence of their cardiovascular sympathoexcitatory function. Evoked responses during stimulation of the splanchnic nerve were inhibited by 49 +/- 6% (n = 7) with EA and by 46 +/- 4% (n = 6) with MA, indicating that the extent of inhibitory effects of the two modalities were similar. Inhibition lasted for 20 min after termination of EA or MA. Cardiovascular premotor rVLM neurons responded to 2-Hz electrical stimulation at P 5-6 and to a lesser extent to 10-, 20-, 40-, and 100-Hz stimulation (53 +/- 10, 16 +/- 2, 8 +/- 2, 2 +/- 1, and 0 +/- 0 impulses/30 stimulations, n = 7). These results indicate that rVLM premotor sympathetic cardiovascular neurons that receive convergent input from the splanchnic and median nerves during low-frequency EA and MA are inhibited similarly for prolonged periods by low-frequency MA and EA.     

Integration of ascending and descending inputs in the auditory midbrain of anurans.

In anurans, the midbrain torus semicircularis is involved in auditory processing and audio-motor integration. In this study, we examined the influence of descending forebrain projections on the auditory response properties and hence the audiomotor transmission of mesencephalic interface neurons. In order to investigate response integration, we performed intracellular recordings from torus neurons in an isolated brain preparation of Discoglossus pictus and Bombina orientalis and stimulated the auditory nerve, striatum, and the dorsal thalamus electrically with single pulses. Stimulation of all three sites could evoke responses in torus neurons that were either excitatory, inhibitory, or a mixture of both, with durations of up to several hundred milliseconds. Further, striatum and thalamus were activated by pulse trains (10-20 Hz, 50 pulses) immediately before stimulating the auditory nerve with single pulses. Thus, responses of torus neurons to "auditory" input were facilitated or suppressed for up to 2 min by striatum stimulation or only suppressed by thalamus stimulation. Intracellular labeling of recorded neurons revealed that response modulation by descending input mostly occurred in laminar nucleus neurons. These results suggest that descending forebrain projections to mesencephalic audiomotor interface neurons may play an important role in modifying acoustically guided behavior in anurans.     

Response characteristics of vibration-sensitive neurons in the midbrain of the grassfrog,Rana temporaria

Summary European grassfrogs (Rana temporaria) were stimulated with pulsed sinusoidal, vertical vibrations (10–300 Hz) and the responses of 46 single midbrain neurons were recorded in awake, immobilized animals.Most units (40) had simple V-shaped excitatory vibrational tuning curves. The distribution of best frequencies (BF's) was bimodal with peaks at 10 and 100 Hz and the thresholds ranged from 0.02 to 1.28cm/s² at the BF.Twenty-three neurons showed phasic-tonic and 11 neurons phasic responses. The dynamic range of seismic intensity for most neurons was 20–30 dB.In contrast to the sharp phase-locking in peripheral vibration-sensitive fibers, no phase-locking to the sinusoidal wave-form was seen in the midbrain neurons. The midbrain cells did not respond at low stimulus intensities (below 0.01–0.02 cm/s²) where a clear synchronization response occurs in saccular fibers.Six midbrain neurons had more complex response characteristics expressed by inhibition of their spontaneous activity by vibration or by bi-and trimodal sensory sensitivities.In conclusion, the vibration sensitive cells in the midbrain of the grassfrog can encode the frequency, intensity, onset and cessation of vibration stimuli. Seismic stimuli probably play a role in communication and detection of predators and the vibration-sensitive midbrain neurons may be involved in the central processing of such behaviorally significant stimuli.Abbreviation BF best frequency     

Neural response directionality correlates of hair cell orientation in a teleost fish

The otolithic end organs in the ears of teleost fishes play important roles in hearing. Although previous studies have shown that afferent fibers innervating otolithic organs are directionally sensitive to acoustic stimulation, no study has demonstrated that directionality of the otolithic afferent neurons derives directly from morphological polarity of the hair cells that they innervate. In this study we investigated whether or not there exists such a structure and function relationship in one of the otolithic organs, the saccule, by using intracellular and extracellular tracing, histochemistry, and confocal imaging techniques. We observed a variety of morphologies of dendritic terminals of saccular ganglion neurons. Arbor innervation areas of these saccular neurons ranged from 893 microm2 to 21,393 microm2, and the number of dendritic endings fell into a range between 10 and 54. We found that the response directionality of saccular ganglion neurons correlates significantly with the morphological polarization of the hair cells in the regions that they innervate. Therefore, we provide direct evidence to support the hypothesis that fish are able to encode directional information about a sound source, particularly in elevation, using arrays of hair cells in the otolithic organs that are oriented specifically along the sound propagation axis.     

Tachykinin release from rat spinal cord in vitro and in vivo in response to various stimuli

The aim of the present study was to establish an experimental model, previously used in cat, for studying tachykinin release from the rat spinal cord in vivo and to compare the results with those obtained in vitro. Stimulation with pulses of 40 mM potassium or 10 microM capsaicin in the spinal cord superfusion fluid increased the release of substance P (SP)- and neurokinin A (NKA)-like immunoreactivity (LI) both in vivo and in vitro. The amounts of SP-LI and NKA-LI released by potassium in vitro were 1.02 +/- 0.12 and 1.17 +/- 0.22 fmol/mg tissue, respectively. Also the ratio between the amounts released by two consecutive potassium stimulations were similar for SP-LI and NKA-LI. Reversed-phase high performance liquid chromatography of the NKA-LI released in vitro by potassium or capsaicin revealed a major immunoreactive component coeluting with synthetic NKA. Despite the use of highly sensitive radioimmunoassays, basal release of SP-LI and NKA-LI was found only in 9 of 31 in vivo experiments. In these, peripheral electrical stimulation of the sciatic nerves (50 Hz, 50 V and 0.05 ms or 10 Hz, 10 V and 5 ms) induced an increase of the SP-LI and NKA-LI levels in the superfusates. This increase persisted for more than 40 min after a 2 min stimulation. In most experiments, however, no SP-LI or NKA-LI could be detected in the superfusates, neither at basal conditions nor following electrical nerve stimulation. Similarly, no release of SP-LI could be detected in response to various noxious mechanical, thermal or chemical stimuli applied to the skin. The present results demonstrate that the superfused rat spinal cord may be used to study in vivo release of tachykinins in response to intense chemical stimulation of the entire spinal cord. However, the method seems to be less suitable for studies of tachykinin release in response to electrical activation engaging only a few spinal segments or in response to natural noxious stimuli. The results obtained in vitro suggest that SP and NKA are released in equimolar amounts from the spinal cord upon stimulation with potassium.     

Effects of abdominal or cardiopulmonary sympathetic afferents on upper cervical inspiratory neurons

Responses of upper cervical inspiratory neurons (UCINs) to abdominal visceral or cardiopulmonary sympathetic stimulation were studied using extracellular recordings from 213 UCINs in 54 pentobarbital sodium-anesthetized and paralyzed rats. Phrenic nerve activity was used to assess inspiration. The UCINs discharging during inspiration only were mainly in the C(1) segment, whereas phase-spanning UCINs were mostly in the C(2) segment. Phase-spanning activity was typically retained after overventilation or vagotomy. When greater splanchnic nerve (GSN) or cardiopulmonary sympathetic afferent (CPSA) fibers were electrically stimulated, augmented UCIN activity was observed in 65% of cells responding to CPSA stimulation but in only 17% of cells responding to GSN. Response latencies were 10.7 +/- 0.5 and 20.6 +/- 1.5 (SE) ms, respectively. Many augmented responses to CPSA stimulation (64%) and all augmented responses to GSN stimulation were followed by suppression of UCIN discharge (biphasic response). Phrenic nerve activity was suppressed by both GSN and CPSA stimulation, but with shorter latency for the latter (29 +/- 0.7 vs. 14.0 +/- 0.7 ms). Excitation of UCINs using CPSA stimulation occurs more often and by a more direct pathway than for GSN input.     

Developmental changes in neuromuscular transmission in the rat diaphragm.

Neuromuscular transmission was studied in diaphragms from rats of three ages, 4-7 days old, 11-12 days old, and adults with the use of an in vitro phrenic nerve-hemidiaphragm preparation. Each hemidiaphragm was stimulated via either muscle or nerve with 1-s stimulus trains at frequencies from 10 to 100 Hz. The patterns of force development obtained in response to the two routes of stimulation were compared for each group. Diaphragms from adults developed maximum force in response to stimulation of approximately 40 Hz with no significant decrease in force at higher frequencies. Within each stimulus train, once peak force was achieved, it was maintained for the remainder of the stimulus and responses to nerve and muscle stimulation were almost identical. In contrast, diaphragms from 4- to 7-day-old rats developed maximum force at approximately 20 Hz; stimulation at greater than or equal to 60 Hz induced significantly less peak force. This decrease in peak force at higher frequencies was significantly larger for nerve than for muscle stimulation. In addition, during each nerve stimulus train diaphragms from 4- to 7-day-old rats were unable to maintain peak force, which decreased at frequencies greater than 20 Hz. The decrease in force reached approximately 50% of peak at stimulation frequencies greater than or equal to 60 Hz. Diaphragms from 11- to 12-day-old rats showed intermediate responses. Based on the responses to phrenic nerve stimulation, we conclude that the neonatal rat diaphragm shows marked neuromuscular transmission failure that is not seen in the adult.(ABSTRACT TRUNCATED AT 250 WORDS)     

Responses of bulbar neurons to stimulation of locomotor and inhibitory sites in the cat brainstem

Bulbar locomotor and inhibitory sites were located in the pons of mesencephalic decerebellate cats. Rhythmic stimulation of locomotor sites through microelectrodes at the rate of 60 Hz elicited stepping movements in the forelimbs which were halted when the inhibitory sites were rhythmically stimulated. Neuronal response was elicited by single or paired stimulation of locomotor sites at the rate of 1.5 Hz or by applying a series of 2–4 stimuli spaced 2 msec apart to the inhibitory site. Medial neurons generated synaptic responses (postsynaptic potentials or action potentials) to stimulation of the inhibitory site twice as frequently as when the locomotor site was stimulated. Responses in lateral neurons, however, occurred twice as frequently to stimulation of the locomotor site, while IPSP were only observed half as often as EPSP in neurons of both groups. In neurons excited by stimulation of the locomotor site, stimulation of the inhibitory site did not normally produce IPSP. Possible mechanisms underlying the halt of locomotion occurring in response to stimulation of the inhibitory site are discussed.Information Transmission Institute, Academy of Sciences of the USSR, Moscow. Translated from Neirofiziologiya, Vol. 18, No. 4, pp. 525–533, July–August, 1986.     

Calcium-induced calcium release contributes to somatic secretion of serotonin in leech Retzius neurons

We analyzed the contribution of calcium (Ca2+)-induced Ca2+ release to somatic secretion in serotonergic Retzius neurons of the leech. Somatic secretion was studied by the incorporation of fluorescent dye FM1-43 upon electrical stimulation with trains of 10 impulses and by electron microscopy. Quantification of secretion with FM1-43 was made in cultured neurons to improve optical resolution. Stimulation in the presence of FM1-43 produced a frequency-dependent number of fluorescent spots. While a 1-Hz train produced 19.5+/-5.0 spots/soma, a 10-Hz train produced 146.7+/-20.2 spots/soma. Incubation with caffeine (10 mM) to induce Ca2+ release from intracellular stores without electrical stimulation and external Ca2+, produced 168+/-21.7 spots/soma. This staining was reduced by 49% if neurons were preincubated with the Ca2+- ATPase inhibitor thapsigargin (200 nM). Moreover, in neurons stimulated at 10 Hz in the presence of ryanodine (100 microM) to block Ca2+-induced Ca2+ release, FM1-43 staining was reduced by 42%. In electron micrographs of neurons at rest or stimulated at 1 Hz in the ganglion, endoplasmic reticulum lay between clusters of dense core vesicles and the plasma membrane. In contrast, in neurons stimulated at 20 Hz, the vesicle clusters were apposed to the plasma membrane and flanked by the endoplasmic reticulum. These results suggest that Ca2+-induced Ca2+ release produces vesicle mobilization and fusion in the soma of Retzius neurons, and supports the idea that neuronal somatic secretion shares common mechanisms with secretion by excitable endocrine cells.     

Cardiac sympathetic nerve stimulation does not attenuate dynamic vagal control of heart rate via alpha-adrenergic mechanism

Complex sympathovagal interactions govern heart rate (HR). Activation of the postjunctional beta-adrenergic receptors on the sinus nodal cells augments the HR response to vagal stimulation, whereas exogenous activation of the presynaptic alpha-adrenergic receptors on the vagal nerve terminals attenuates vagal control of HR. Whether the alpha-adrenergic mechanism associated with cardiac postganglionic sympathetic nerve activation plays a significant role in modulation of the dynamic vagal control of HR remains unknown. The right vagal nerve was stimulated in seven anesthetized rabbits that had undergone sinoaortic denervation and vagotomy according to a binary white-noise signal (0-10 Hz) for 10 min; subsequently, the transfer function from vagal stimulation to HR was estimated. The effects of beta-adrenergic blockade with propranolol (1 mg/kg i.v.) and the combined effects of beta-adrenergic blockade and tonic cardiac sympathetic nerve stimulation at 5 Hz were examined. The transfer function from vagal stimulation to HR approximated a first-order, low-pass filter with pure delay. beta-Adrenergic blockade decreased the dynamic gain from 6.0 +/- 0.4 to 3.7 +/- 0.6 beats x min(-1) x Hz(-1) (P < 0.01) with no alteration of the corner frequency or pure delay. Under beta-adrenergic blockade conditions, tonic sympathetic stimulation did not further change the dynamic gain (3.8 +/- 0.5 beats x min(-1) x Hz(-1)). In conclusion, cardiac postganglionic sympathetic nerve stimulation did not affect the dynamic HR response to vagal stimulation via the alpha-adrenergic mechanism.     

Nerve,spinal cord and brain somatosensory evoked responses: a comparative study during electrical and magnetic peripheral nerve stimulation

Somatosensory evoked potentials (SEPs) and compound nerve action potentials (cNAPs) have been recorded in 15 subjects during electrical and magnetic nerve stimulation. Peripheral records were gathered at Erb's point and on nerve trunks at the elbow during median and ulnar nerve stimulation at the wrist. Erb responses to electrical stimulation were larger in amplitude and shorter in duration than the magnetic ones when ‘electrical’ and ‘magnetic’ compound muscle action potentials (cMAPs) of comparable amplitudes were elicited. SEPs were recorded respectively at Cv7 and on the somatosensory scalp areas contra- and ipsilateral to the stimulated side. SEPs showed a statistically significant difference in amplitude only for the brachial plexus response and for the ‘cortical’ N20-P25 complex; differences were not found between the magnetic and electrical central conduction times (CCTs) or for the peripheral nerve response latencies. Magnetic stimulation preferentially excited the motor and proprioceptive fibres when the nerve trunks were stimulated at motor threshold intensities.     

VIP and noncholinergic vasodilatation in rabbit submandibular gland

The effect of parasympathetic nerve activation on rabbit submandibular gland (SMG) blood flow and saliva secretion were studied before and after systemic administration of atropine or hexamethonium. The parasympathetic fibers were stimulated electrically (2 and 15 Hz, 10 V, 1 msec) at the plexus around the submandibular salivary duct or at the chorda lingual nerve. In untreated animals, stimulation of parasympathetic fibers caused a frequency-dependent increase of salivary secretion and blood flow in the SMG. Atropine treatment completely abolished saliva secretion at 2 Hz and 15 Hz and the increase in SMG blood flow during stimulation at 2 Hz. Although atropine significantly reduced the vasodilatory response at 15 Hz, the highest blood flow measured under such circumstances was still about 2.5 times the prestimulation value. After hexamethonium administration no blood flow increase or saliva secretion was seen upon chorda lingual stimulation. The concentration of vasoactive intestinal polypeptide (VIP)-like immunoreactivity in the venous effluent of the SMG increased during nerve stimulation. Atropine significantly reduced, and hexamethonium abolished this VIP-output elicited by parasympathetic nerve stimulation. Local infusion of VIP, peptide histidine isoleucine (PHI) and substance P all caused atropine-resistant vasodilation but no salivation. The present data suggest that VIP and possibly PHI play a role in the atropine-resistant vasodilatation in rabbit submandibular gland elicited by parasympathetic nerve stimulation. The contribution of sensory mediators such as substance P released by stimulation of afferent nerves in the chorda lingual nerve to the salivary and vasodilatory responses seems to be of minor importance in the rabbit submandibular gland.     

Cholinergic nerves stimulate mucociliary transport,ciliary activity,and mucus secretion in the frog palate

Summary Mucociliary transport, ciliary activity, and mucus secretion were studied in the palate of the frog Rana pipiens by direct observation, stroboscopic synchronization of ciliary beating, and histochemistry. Excised palates were studied in vitro, and intact palates were studied in vivo. Electrical stimulation of the glossopharyngeal nerve in vivo or of the palatine nerve in vitro stimulated all three activities. The effect was mimicked by acetylcholine and pilocarpine, enhanced by physostigmine, and blocked by atropine but unaffected by d-tubocurarine. Stimulation increased the number of cilia beating and their rate of beating, the number of goblet cells secreting and, for small acidic cells, the amount of mucus secreted, and the rate and extent of particle transport. The response to tactile stimulation was locally restricted in vitro but widespread in vivo. It was concluded that, although there is a low basal rate of mucus secretion and ciliary activity that is independent of nervous control, stimulation of these activities in the intact animal is mediated through the central nervous system and cholinergic nerves to the palate.Supported in part by Grant HL-16730 from the U.S. Public Health Service     

A vagal nerve branch controls swallowing directly in the seawater eel

By developing a new in vivo method to evaluate the esophageal closure, which reflects inhibition of swallowing, we demonstrate that the vagal X1 branch projected from the glossopharyngeal-vagal motor complex (GVC) controls the upper esophageal sphincter (UES) muscle directly. Although eel vagal nerve consisted of five branches, other branches (X2, X3, X4 and X5) did not influence the esophageal pressure. When the X1 nerve branch was stimulated electrically, the balloon pressure in the UES area increased with optimum frequency of 20 Hz. Since similar optimum frequency was observed both in the pithed eel and in the isolated UES preparation, such characteristic of X1 nerve is not due to anesthetic used during experiment. As the isolated UES preparation consists of muscle cells and nerve terminals, and as the optimum frequency of the nerve terminal is identical with that of the X1 branch, it is most likely that the X1 nerve branch is identical with the nerve terminals within the UES preparation. On the other hand, since the GVC neurons fire spontaneously at around 20 Hz, the optimum frequency of 20 Hz means that the eel UES is usually closed vigorously and relaxed only when the GVC neuron is inactivated. The effect of X1 stimulation was inhibited by curare, but not by atropine, indicating that the X1 nerve branch releases acetylcholine, which acts on the nicotinic receptor on the UES striated muscle. Beside vagal nerve X1 branch, spinal nerve SN2, SN3 and SN4 also contributed to the UES closure, but SN1 did not influence the UES movement. However, since the efficacy of these spinal nerve stimulations is about 1/10 of that by vagal X1 branch, the eel UES may be controlled primarily by a vagal nerve X1 branch, and secondarily by spinal nerves (SN2, SN3 and SN4).     

Response of the saccule to the direct vibratory stimulation of the macula in frogs]

Direct stimulation of the frog's saccular macula shows that the saccular fibers are sensitive to vibrations between 10(-1) (at least) and 8.10(3) Hz and that their response depends on 1) the frequency of the vibration, 2) the origin of the fiber in the macula.